The nervous system collects and processes information, analyzes it, and generates
coordinated output to control complex behaviors. The nervous system also is partly
responsible for homeostasis. It works in conjunction with the endocrine system by
employing nerve impulses and by responding rapidly to stimuli to adjust body processes.

The nervous system is broken down into two major systems the Central NervousSystem
and the Peripheral
Nervous System. These two systems are in control of sensory input, integration,
and motor output. The Central Nervous system is made up of mainly the brain and spinal
cord. The CNS is in control of the input from sensory receptors from the chemical and
electrical signals sent from the PNS. The CNS takes the information and integrates it,
then sends out the necessary motor output to the effector cells of the body.

The PNS is divided into two systems as well, the Somatic Nervous System,
and the Autonomic
Nervous System. The SNS consists of sensory neurons that send information from
cutaneous and special sensor receptors in the head, body wall, and extremities to the CNS
where the information is integrated and sent back out via motor neurons to skeletal
muscles. The sensory neurons convey input from receptors from senses like vision, hearing,
taste, smell and others. They also convey input from proprioceptors and general somatic
receptors (pain, temperature, and tactile sensations). Motor neurons innervate skeletal
muscle and produce voluntary movement. The ANS sends information from sensory neurons to
viscera of the CNS. In the ANS the CNS sends information through motor neurons to smooth
muscles, cardiac muscles and glands. The ANS is controlled by the hypothalamus and medulla oblongata of
the brain, which regulate the smooth muscle, cardiac muscle, and specific glands.

The output portion of the autonomic nervous system further breaks down into two
divisions, the sympathetic
and parasympathetic.
The parasympathetic division is the energy control center; it regulates energy through
conservation and restoration. The sympathetic division is in charge of the flight of fight
responses of the body. It is in charge of the excitatory processes of the body. This
division is in charge of the usage of energy.

In summary, the nervous system has three overlapping functions. These functions are
sensory input, integration, and motor output. Input is the conduction of signals from
sensory receptors to integration centers of the nervous system. Integrating the
information requires that the sensations triggered by environmental stimulation of
receptors be interpreted and associated with appropriate responses of the body. Motor
output is the conduction of signals from the brain or other processing center of the
nervous system to effector cells. Effector cells are the muscle cells or gland cells that
actually perform the bodys responses to stimuli.

Neurons come in a variety of sizes and shapes, but they all have basically the same
functional regions. Signals from other neurons or sensory cells are
received on the dendrites and cell body (soma) and cause localized changes in membrane
polarization. The electrical changes spread across the cell body and are combined at the axon hillock, located at the base of the axon. This is the region responsible for generating
action potentials, which then travel quickly along the axon and its branches to the
terminal knobs - small swollen areas at the end of the axon branches. Here the neuron
interfaces with other cells at junctions called synapses through which signals are
transmitted. Neurons that bring signals to the central nervous system (the brain and
spinal cord) are referred to as sensory neurons, whereas those that carry signals from the
central nervous system to the rest of the body are called motor neurons. Within the
central nervous system there are also small, highly branched interneurons that help
neurons communicate with one another. The axons of some vertebrate neurons have a fatty
myelin sheath formed by supporting Schwann cells. This sheath helps support the fine axon
and also increases the conduction velocity of nerve impulses (action potentials) - (see question below).

The supporting cells outnumber neurons tenfold to fiftyfold in the nervous system.
They are essential for the structural integrity of the nervous system and for the normal
functioning of neurons. They provide intimate structure and perhaps metabolic support for
neurons.

There are different types in the body. Oligodendrocytes, are located in the CNS.
Schwann cells of the peripheral nervous system wrap each axon in an insulating myelin
sheath, which contributes to assuring reliable and rapid transmission of action potentials.

Although some glial cells have
voltage-gated ion channels in their membranes, glial cells generally do not produce action
potentials and their role in the nervous system has long been a puzzle. One suggestion has
been that glial cells help to regulate the concentration of K+ and the pH in the
extracellular fluid of the nervous system. Glial cell membranes are highly permeable to K+
and adjacent glial cells are often electrically coupled by junctions that allow K+ to flow
between them. This flux permits glial cells to take up and redistribute extracellular K+,
which otherwise could build up to high concentrations in narrow extracellular spaces
following activity in neurons. Glial cells also may take up neurotransmitter molecules
from the extracellular space, thereby limiting the amount of time a neurotransmitter could
be active at synapses.

All living cells maintain some differences between the concentration of ions and other
solutes inside and outside the cell. This is the purpose of a cell membrane in the first
place - to help maintain differences between the inside and the outside. The combination
of differences in the chemical concentrations of solutes and the distribution of the
charges of the ions establishes an electrochemical gradient between the inside and outside
of the cell membrane. If the chemical concentration gradients are
offset by a difference in the distribution of electrical charges so that no net movement
of ions takes place, we have a condition known as electrochemical equilibrium.

In this equilibrium condition any tendency of solutes to diffuse down their respective
concentration gradients (from high to low concentration) is regulated by not only the
difference in chemical concentration and by their electrical attraction to or repulsion by
other charged molecules, but also their ability to pass through the cell membrane. Lipid
soluble molecules can pass through the cell membrane. Molecules that are not lipid soluble
must pass through channels in the membrane, and are therefore limited by the size and
number of these channels.

When in electrochemical equilibrium, living cells have a net negative charge along the
inside of the cell membrane. This is due primarily to the surplus of large negatively
charged molecules, such as proteins, in the cytoplasm. These large molecules cannot
diffuse down their concentration gradient and move to the outside of the cell because they
are too big to pass through small channels in the cell membrane. The surplus of these
large negatively charged ions inside the cell tends to repel other negatively charged
ions, such as chloride, resulting in a higher concentration of these smaller negatively
charged ions on the outside of the cell. Meanwhile, an ion pump actively transports
positively charged sodium ions from the inside to the outside of the cell, creating a
surplus of sodium ions outside the cell membrane. The ion pump does exchange some
potassium (also positively charged) for the sodium, but it is an uneven exchange, with the
amount of sodium leaving the cell exceeding the amount of potassium being brought in.
Sodium and potassium ions are small enough to slowly diffuse down their chemical
concentration gradients by passing through small channels in the cell membrane, but the
ion pump keeps up with this slow leakage and maintains the electrochemical equilibrium.
The result of all of this is that the ion pump maintains an equilibrium condition in which
there is more sodium outside the cell, more potassium inside the cell, and the inside of
the cell has a net negative charge with respect to the outside.

This balance between electrical and chemical gradients and the regulation of the
passage of these ions back and forth is what distinguishes a living cell from an inert bag
of ions. It also permits certain cells to respond to stimuli.

The difference in electrical charge between the two sides of a cell membrane is known
as the membrane potential. When a cell is not being stimulated, and is therefore "at
rest", we refer to the membrane potential as the resting potential. If a cell becomes
stimulated, perhaps by some mechanical or chemical disturbance, the permeability of the
cell membrane can be momentarily affected resulting in a temporary change in the
electrochemical balance. Most cells in an animal's body don't show much of a response to
such a stimulus, other than to reestablish electrochemical equilibrium. Some cells,
however, show a dramatic, active response at the level of the cell membrane that results
in a momentary but striking reversal of charge distribution known as an action potential.
This ability to generate action potentials is what makes certain cells excitable, and it
is these excitable cells that are responsible for sensory, nerve, and muscle function.

Stimuli alter the permeability of the cell membrane by causing ion channels to open.
For example, a slight stimulus may cause some sodium channels to open. With this route now
available, sodium ions flow rapidly into the cell, driven by their own concentration
gradient and the attraction of the excess negative ions. The sodium-potassium pump still
is transporting some sodium out of the cell, but it is overwhelmed by this rapid influx of
sodium ions. This results in a decrease in the electrical potential difference between the
inside and the outside of the cell, so the membrane potential decreases (depolarization).
If the sodium channels now close, the ion pump will reestablish electrochemical
equilibrium.

In excitable cells, the sodium gates may not close right away, however. If the membrane
potential becomes altered to a critical level, known as the "threshold
potential", more sodium gates will open, thereby allowing even more sodium to flow
into the cell even more rapidly. These sodium channels open in response to voltage change
across the membrane. Therefore, they are referred to as voltage-regulated channels. As
more sodium flows in, more sodium gates open, and so on. This example of positive feedback
to rapidly allow more sodium into the cell is called the Hodgkin cycle. The net result of
this rapid influx of sodium ions is that the inside of the cell has now become positive
with respect to the outside. In this extremely depolarized condition the cell membrane
cannot respond to another stimulus until its original polarity is reestablished. This
extreme depolarization event is very brief, however, because the sodium gates close when
the membrane potential reaches a certain point, preventing any further sodium influx. The
cell membrane then "repolarizes" by opening potassium gates (also
voltage-regulated) and allowing potassium ions to flow out, driven by their concentration
gradient and the repulsion of the positively charged sodium ions that are now abundant
inside the cell . The sodium-potassium pump could repolarize the membrane, but it would
take too long to be biologically useful. This rapid repolarization of the cell membrane
reestablishes the resting potential of the cell, and puts the cell in a condition where it
now can respond to another stimulus. Gradually, the sodium-potassium exchange pump will
move sodiums out and potassiums in, thereby reestablishing the original ion distribution.
This brief exchange of sodium and potassium ions only affects those ions
immediately adjacent to the cell membrane. It does not have a significant impact on
the overall intracellular and extracellular concentration of sodium or potassium.

The rapid depolarization and repolarization of the membrane of an excitable cell is
called an "action potential", and it is important to understand this series of
events in order to understand the events involved in the functioning of the nervous
system.

The reception of signals from other neurons or sensory cells causes a small change in
the membrane potential at the site of the synapse. These changes in membrane potential are
proportional to the intensity of the stimulus (graded potentials) and are referred to as
postsynaptic potentials (PSPs) because they occur on the postsynaptic (receiving)
membrane. These PSPs spread outward from the synapse and across the membrane of the
dendrites and cell body. As they spread they may encounter and combine with PSPs from
other synaptic junctions that also are being stimulated. (At any given moment a neuron may
be receiving stimuli from many different sources.) The PSPs are continually being combined
in the axon hillock, and if at any given moment the sum of all of the PSPs is sufficient
to bring the membrane potential of the axon hillock to its threshold, an action potential
is generated. If the summation of the PSPs fails to reach threshold, an action potential
will not be generated.

No - postsynaptic potentials can be either excitatory (EPSPs) or inhibitory (IPSPs).
EPSPs depolarize the postynaptic membrane, often by increasing the inward flow of sodium,
thereby increasing the number of positive charged ions on the inside of the cell membrane.
This results in a decrease in the voltage difference across the membrane, bringing the
membrane potential of the axon hillock closer to threshold. This increases the likelihood
that an action potential will be generated, which is why these depolarizing PSPs are
called excitatory.

IPSPs, however, hyperpolarize the postsynaptic membrane, often by increasing the
leakage of potassium ions out of the cell or increasing the flow of chloride ions into the
cell. This increases the voltage difference across the membrane, and pushes the membrane
potential further from the threshold voltage. This decreases the likelihood that an action
potential will be generated, which is why these hyperpolarizing PSPs are called
inhibitory.

The generation of an action potential involves the rapid depolarization and
repolarization of the cell membrane. If an action potential is generated, the Hodgkin
cycle assures that it is of maximal force, regardless of whether the sum of all PSPs
greatly exceeded threshold or was just barely strong enough to reach threshold. This gives
action potentials and "all-or-none" property. In other words, if threshold is
reached or exceeded, the action potential will be maximal; if threshold is not reached an
action potential will not be generated. There is no in-between at the level of the
individual neuron. (Nerves are bundles of neurons and can show different levels of
response because the individual neurons may exhibit different thresholds.)

If an action potential is generated at the axon hillock it now will spread quickly
along the axon as a "wave" of depolarization. An important property of action
potentials is that they do not lose intensity as they travel because they are regenerated
as they move along the axon. This regeneration of the action potential occurs because the
depolarization of one region of the axon depolarizes the adjacent region and brings it to
its threshold, thereby generating another action potential. In axons
that lack a fatty, insulating myelin sheath, this propagation of the action potential
occurs continuously along the length of the axon. The opening and closing of the
appropriate ion gates slows the signal down somewhat, but the signal's intensity does not
diminish as it travels.

Most vertebrate axons do have a myelin sheath, however, which helps the signal move
more quickly by limiting action potential regeneration to the nodes of Ranvier.
Action potentials can occur only where the axon cell membrane is in close contact with
extracellular fluid. Therefore areas of the axon covered with a myelin sheath cannot
regenerate action potentials. They can, however, rapidly conduct an electrical field to
the next exposed section of axon membrane - the next node of Ranvier. Here the action
potential is regenerated and transmitted further along the axon. Because fewer
regeneration events take place, the signal moves more quickly than if the myelin were not
present. The myelin sheath, then, increases the conduction velocity of an axon.

Another way to increase conduction velocity is to increase the diameter of an axon. As
in electrical wires, there is some resistance to current flow along the periphery.
Increasing the diameter of a wire increases the proportional cross-sectional area of the
wire that is not in direct contact with the periphery, thereby decreasing the effect of
peripheral resistance. In other words, more charge can flow quickly because proportionally
less is slowed by peripheral resistance. Large diameter axons, therefore, can transmit
action potentials faster than those with small diameters. Some invertebrates have very
large diameter non-myelinated axons responsible for rapid reflexes. For example, the
"giant axon" associated with the stellate ganglion of squid is responsible for
the rapid contraction of the mantle which provides jet propulsion for squid escaping a
predator.

Large diameter axons with myelin sheaths can transmit action potentials extremely fast.
The Mauthner cells in fishes have among the highest conduction velocity known among the
vertebrates (50 to 100 m/s). These large-diameter, myelinated neurons are responsible for
the startle response that helps a fish rapidly curl its body and flick its tail, resulting
in rapid movement away from a stimulus (think of this the next time that you tap on the
side of an aquarium).

When an action potential reaches the end of a neuron, the signal is transmitted to
another cell, such as a muscle cell or another neuron. The area of signal transmission is
called a synapse, and these come in two general varieties - electrical and chemical. In electrical synapses the presynaptic
(transmitting) and postsynaptic (receiving) membranes are in direct contact with one
another and small channels permit ions to flow through almost as if there was no barrier
at all. Electrical synapses, therefore, transmit signals very rapidly.

Chemical synapses, which are more
common, require the release of a chemical transmitter substance by the presynaptic
membrane in order to stimulate the postsynaptic membrane. There are two types of chemical
syapses - fast (direct) and slow (indirect). In both types, the arrival of the action
potential at the presynaptic knob results in an opening of calcium channels on the
presynaptic membrane. The resulting influx of calcium ions causes vesicles of transmitter
substance to bind to the presynaptic membrane and release their contents.

In a fast chemical synapse, molecules of transmitter substance diffuse from the
presynaptic membrane across the synaptic cleft and bind to receptor molecules on the
postsynaptic membrane. These receptor proteins also form the ion channel, and the binding of the neurotransmitter directly alters the configuration of the
proteins and opens the ion channels of the postsynaptic membrane. (This is why these
channels are referred to ligand-gated channels.) This allows molecules such as sodium to
move across the membrane and alter its membrane potential, creating postsynaptic
potentials.

In a slow chemical synapse, the binding of the neurotransmitter to a receptor on the
cell membrane activates nearby G-proteins. This catalyzes a series of reactions that
results in the release of another molecule (a second messenger) which binds to the
proteins that form an ion channel. This alters the configuration of
the channel, thereby opening it and allowing ions to flow through. This is an indirect,
and therefore slower, mechanism because it requires a series of biochemical reactions.
Transmission at slow chemical synapses is slower, longer lasting, and may be more
widespread spatially than the rapid, localized and immediate response seen at fast
chemical synapses. Both types of synapses may be found on the dendrites or soma of a
receiving neuron, and the effects of slow synapses may play a role in modulating the
effects of a fast synapse by altering the membrane potential of the postsynaptic membrane.

Molecules of transmitter substances in the synaptic cleft and those bound to receptor
molecules on the postsynaptic membrane are quickly broken down by enzymes. This is
important for two reasons. First, the resulting components are taken up by the presynaptic
membrane and recycled to produce more transmitter substance. Second, the postsynaptic
membrane must be relieved of the stimulation by the transmitter substance molecules so
that it can reestablish its resting potential. If transmitter substance molecules remained
bound to their receptor sites, the associated ion channels would remain open and the
receiving cell could not function properly.

Understanding the cellular mechanisms of the nerve function helps us understand ways in
which certain neurotoxins have their effects. Inhibition of proper nerve function can lead
to death, often due to respiratory paralysis. Tetrodotoxin, the toxin from the viscera of
puffer fish (Tetraodontiformes) binds to the extracellular surface of the proteins that
make up sodium channels. This blocks the sodium channel, thereby inhibiting the proper
function of neurons or other excitable cells. Saxitoxin, a paralytic
shellfish toxin produced by some dinoflagellates responsible for "red tides",
has the same specific effect as tetrodotoxin. The venom of the krait, one of the highly
poisonous cobra snakes, contains alpha-bungarotoxin, which binds irreversibly to a
particular group of neurotransmitter receptors, thereby inactivating them. The toxin
responsible for botulism, which is produced by the bacterium Clostridiumbotulinum,
prevents the release of an important group of neurotransmitters from their vesicles,
thereby preventing neurotransmission.

The Endocrine System

The endocrine system is the internal system of the body that deals
with chemical communication by means of hormones,
the ductless glands that secrete the hormones, and those target cells that respond to
hormones. The endocrine system functions in maintaining the basic functions of the body
ranging from metabolism to growth. The endocrine system functions in long term behavior
and works in conjunction with the nervous system in regulating internal functions and
maintaining homeostasis.

Hormones are the chemical messengers released by specialized endocrine cells or
specialized nerve cells called neurosecretory cells. Hormones are released by the endocrine system
glands into the bodys fluids, most often into the blood and transported throughout
the body. Hormones are specified by their different chemical structures which can be
classified into four categories

Amines: are small molecules originating from amino acids. Examples of this are
epineprine and thyroid hormones.

Steroid hormones: are cyclic hydrocarbon derivatives synthesized in all instances from
the precursor steroid cholesterol. Examples of this are testosterone and estrogen.

Peptide and Protein hormones: are the largest and most complex hormone. Example of this
is insulin.

Hormones drive the endocrine system and without them the body could not function.
Hormones are the communicators of the endocrine system and are responsible for maintaining
and controlling cellular activity.

Hormones regulate bodily functions and are specific in what responses they elicit. As
hormones are released into the bloodstream they can only initiate responses in target cells, which are
specifically equipped to respond. Each hormone due to its chemical structure is recognized
by those target cells with receptors compatible with their structure. Once a hormone is
released, the first step is the specific binding of the chemical signal to a hormone
receptor, a protein within the target cell or built into the plasma membrane. The receptor
molecule is essential to a hormones function. The receptor molecule translates the hormone
and enables the target cell to respond to the hormones chemical signal. The meeting of the
hormone with the receptor cell initiates responses from the target cell. These responses
vary according to target cell and lipid solubility.

Hormones are either lipid-soluble or lipid-insoluble, depending on their biochemical
structure. The lipid solubility of the hormone determines the mechanism by which it
can affect its target cell.

Lipid-soluble hormones are able to penetrate through the cell membrane and bind to
receptors located inside the cell. Such hormones diffuse across the plasma membrane and
target those receptor cells found within the cytoplasm. Lipid-soluble hormones target the
cytoplasmic receptors which readily diffuse into the nucleus and act on the DNA,
inhibiting and stimulating certain proteins. DNA function is of great influence over the
cellular activities of the body and therefore such hormonal-DNA interaction can have
effects as long as hours and in some cases days. Two known types of lipid soluble hormones
are steroids and thyroid hormones. Both travel over long courses of time via the
bloodstream and both directly effect DNA functions.

Those hormones which are lipid-insoluble are unable to penetrate through the plasma
membrane and function with their target cells in a much different and complex manner.
Lipid-insoluble hormones must bind with cell-surface receptors which follow a different
path involving a second messenger. The hormone's inability to penetrate the membrane
requires a second messenger which translates the outer message and functions within the
cell.

Once a lipid-insoluble hormone binds with a cell surface receptor, its signal is
translated into the cell by specific secondary messengers. There are three known and
accepted secondary messengers which vary in structure and function, but all three carry
out the external signal internally. The three known secondary messengers are (1) cyclic
nucleotide compounds (cNMPs), cAMP, and
cGMP; (2) inositol phospholipids; and (3) Ca2+ ions. After a hormone binds with a receptor
molecule it via a transducer protein sends the hormones signal through the membrane. The
protein receptor initiates the formation of a second messenger, whether it be it be cAMP
or an inositol phospholipid, which then binds to an internal regulator. The internal
regulator controls the target cells response to the hormone's signal.

Each different type of secondary messenger evokes different responses by those cells
they affect. cAMP has wide range of tissues it targets and those responses it elicits.
cAMP pathways can increase the heart rate and force a contraction in a heart, it can
decrease lipid breakdown in fat cells, and it can stimulate resorption of water in a
kidney. An inositol phospholipid pathway can initiate breakdown of liver glycogen and DNA
synthesis in fibroblasts. Ca2+ pathways are linked to initiating responses in striated
muscles most notably contraction. These responses, however, are short lived responses;
much shorter then those by lipid soluble affected cells. Although the cellular mechanisms
of hormones vary according to solubility and first and second messengers, such hormones
function in eliciting responses from their target cells.

Hormones more or less function as a stimulant, promoting an action in a target cell
which can be magnified in stimulating organs or even systems. Hormone stimulation varies
from growth and metabolic functions to ova and sperm production.

There are two ways in which the endocrine system affects the rest of the organism. The
first method of transmission, is called local signaling. This is when regulators are
released by a gland or cell into the interstitial fluids and are absorbed by nearby cells.
The second method of transmission is called long distance signaling. Long distance
signaling takes place when an endocrine cell or neurosecretory cell releases hormones into
the bloodstream. Once in the bloodstream the hormones travel to the receptor cell. When
they reach their destination the receptor cell integrates the signal and reacts to its
design.

Growth factors affect the development of new cells. There are specific hormones that
correspond with the development of specific cells. For example, epidermal growth factor is
required to grow epithelial cells. The rate of growth can also be affected, for example an
experiment on fetal mice was done to see if rate of growth of skin would change with an
influx of hormones. It was found that by injecting the fetal mice with EGF that skin
developed faster.

The hypothalamus and pituitary gland are two parts of
the brain that have important roles in integrating the nervous and endocrine system. The
hypothalamus is found in the lower part of the brain in the midbrain where it functions in
receiving messages from nerves and integrating that into endocrine gland responses. The
hypothalamus is more or less the communication link between the nervous system and the
endocrine system. The hypothalamus regulates the secretion of various hormones by
controlling the main hormonal gland the pituitary gland

The pituitary gland releases hormones that control many of the endocrine system's
functions. The pituitary gland releases hormones when signaled by the hypothalamus. The
pituitary gland has numerous functions which are performed by its two parts.
Pituitarys two separate parts are essential to the production of many hormones but,
their function in relation to the hypothalamus and endocrine system vary greatly.

The posterior pituitary is an extension of the brain and secretes two types of
hormones, oxytocin and antidiuretic hormone(ADH), both of which are produced by the
hypothalamus and released into the posterior pituitary. Neurosecretory cells in the
hypothalamus produce oxytocin and ADH and are transported down an axon to the posterior
pituitary where it is stored. The posterior pituitary releases these hormones when needed
via the bloodstream and bind to their target cells. The posterior pituitaries hormones
elicit specific responses from the kidneys, by means of ADH, and the mammary glands, by
means of oxytocin. ADH acts directly on the ability of the kidneys to reabsorb water,
whereas oxytocin causes mammary glands to release milk.

The anterior pituitary also relies on the hypothalamus to control and regulate its
hormonal release, but in a less direct manner. The release of hormones by the
anterior pituitary is driven by neurosecretory cells located in the hypothalamus. When the
hypothalamus receives a signal for the need of a hormone produced by the anterior
pituitary, it sends releasing
hormones through short portal vessels and into a second capillary network within the
anterior pituitary, where it acts on a specific hormone. Besides releasing stimulatory
hormones the hypothalamus also releases inhibiting hormones which prevent the release of
certain hormones from the anterior pituitary. The anterior pituitary produces and releases
several different hormones with many different functions. Its hormones range from growth
hormones that act on bones, to prolactin which stimulates mammary glands. A unique
function of those hormones released by the anterior posterior, is that some of them act on
other endocrine glands and signal them to produce and release other hormones. Tropic
hormones are responsible for this, such as thyroid stimulating hormone which stimulates
the thyroid and its production of hormones.

Pheromones are chemical signals
that function as external communicators whereas hormones are internal. Pheromones
communicate between separate individuals, not within one individual as hormones do.
Pheromones are communicating chemicals that act between animals of the same species.
Pheromones are dispersed into the environment and are used in attraction, defense, and
marking territories. Pheromones play a great role in the insect world, but their
importance in human interaction is disputed. Some scientist question the presence of
chemical influence on human behavior while an entire industry, the fragrance industry,
bases its existence on the appreciation for external scents. Pheromones most likely play a
hidden role in the interaction of humans with each other.

The nervous and endocrine systems are related in three main areas, structure, chemical,
and function. The endocrine and nervous system work parallel with each other and in
conjunction function in maintaining homeostasis, development and reproduction. Both
systems are the communication links of the body and aid the bodys life systems to
function correctly and in relation to each other.

Structurally many of the endocrine systems glands and tissues are rooted in the nervous
system, Such glands as the hypothalamus and posterior pituitary are examples of nerve
tissues that influence the function of a gland and its secretion of hormones. Not
only does the hypothalamus secrete hormones into the bloodstream, but it regulates the
release of hormones in the posterior pituitary gland. Those that are not made of nervous
tissue once were. The adrenal
medulla is derived from the same cells that produce certain ganglia.

Chemically both the endocrine and nervous system function in communication by means of
the same transmitters but use them in different ways. Hormones are utilized by both
systems in signaling an example of this can be seen in the use of Norepinephrine.
Norepineprine functions as a neurotransmitter in the nervous system and as an adrenal
hormone in the endocrine system.

Functionally the nervous and endocrine system work hand in hand acting in communicating
and driving hormonal changes. They work in maintaing homeostasis and respond to changes
inside and outside the body. Besides functioning in similar manners they work in
conjunction. An example of this can be seen in a mothers release of milk. When a baby
sucks the nipple of its mother, sensory cells in the nipple sends signals to the
hypothalmus, which then responds by releaing oxytocin from the posterior pituitary. The
oxytocin is released into the bloodstream where it moves to its target cell, a
mammary gland. The mammary gland then responds to the hormones signal by releasing milk
through the nipple. Besides working in conjunction with each other, both systems affect
one another. The adrenal medulla is under control the control of nerve cells, but the
nervous systems development is under the control of the endocrine system.

Growth hormone (GH) is a peptide hormone produced by the
anterior lobe of the pituitary gland in response to GH-releasing hormone from the
hypothalamus. Release of growth hormone is inhibited bysomatostatin, which also is
produced by the hypothalamus. GH enhances the metabolism of fats for energy. It also
enhances amino acid uptake and protein synthesis, which help in growth of cartilage and
bone. Secretion of growth hormone is increased by exercise, stress, lowered blood
glucose, and by insulin.

There are many hormones that in one way or another effect
attitude and behavior, but in the interest ot time and space, this section will mostly
discuss the gonadal, placenta, and thyroid hormones.

A variety of hormones are produced by the gonads and
placenta. Estrogens, such as estradiol, function in the development and maintenance of the
female reproductive tract, in the simulation of the mammary glands, in the development of
secondary sex characteristics, and in the regulation of behavior. Androgens, such as
testosterone, influence the development and maintenance of the male reproductive tract,
secondary sex characteristics, and behavior.

There has been a great deal of interest in the
relationship between hormones and behavior and it has been found that the natural
variation in the amount of hormones present is correlated with variation in behavior. For
example, during the female menstrual period the "average" female shows a
decreased body temperature, decrease in food and water intake, decrease in body weight,
and she becomes sexually receptive. These variations within the body cause the females
behavior to change. It's been found that it can result in changing of mood, performance in
cognitive tasks, sensory sensitivity, and sexual activity. Unfortunately, due to the
possible implications of gender issues this research is controversial. The same can happen
with males. Research has shown that there is some suggestion of a relationship between
androgens, like testosterone, and dominance-related behavior. For example, men with high
levels of testosterone are prone to be more competitive and have a higher level of
aggression.

Thyroid hormones can also influence a person's mood due to
the changes in the thyroid's activity. Little is known about the mechanisms by which
thyroid hormones elevate mood, but it has a connection to the neural functions in the
brain, which have influence over hormone releasal.

Many psychological disorder are directly related to
certain impairments of brain functioning (chemical and hormonal imbalances), while others
are more behaviorally orientated. Affective Disorders, for example, are those in which
there is a disturbance of mood. One form of this disorder is depression which has been
related to a number of hormones like melatonin and thyroid hormones.

Headaches, which can dramatically make a person irritable,
snappy, and emotional can be another consequence of a hormone. During the female menstrual
period, around ovulation time, estrogen rises to a peak. When estrogen is high a message
goes out to produce a hormone called serotonin. This hormone makes the blood vessels in
the brain narrow. This doesn't cause any pain, but when the estrogen, and hence serotonin,
levels drop, blood vessels in the head begin to expand and put pressure on nerves. This
causes the pain you feel when you have a headache.

Seasonal Affective Disorder(SAD) is a seasonal disruption
of mood that occurs during the winter months. Symptoms of it usually begin in the fall
when the day light hours begin to shorten and last until the day light hours begin to
lengthen again in the spring. Some symptoms of SAD are depression, tiredness, increased
appetite (which can lead to weight gain), and irritability. The direct cause for this
disorder is in connection to the hormone melatonin.

The pineal gland, which is located in the center of the
brain, releases a hormone called melatonin. This hormone can accumulate in the
hypothalamus where it can have an effect on long-term releasing factors influencing growth
and reproductive development and also on circannual rhythms (seasonal timing). SAD
is influenced by the latter of those. Very little melatonin is secreted in the
daytime (light) and a great deal is produced at night (dark). Because the winter months
have longer nights there is an extra production of melatonin. Therefore, the level
of melatonin in the body increases. This production of melatonin influences our
overall mood and causes SAD. Unfortunately, there isn't any concrete information on
the exact reasoning to how or why this happens, but there are plenty of ways in which
people try to cure it. For example, artificial lighting.

There have been several experiments that demonstrate that
changes in the level of melatonin in the bodies of seasonally breeding animals affect
their reproductive cycle. Artificial lighting can prolong this breeding activity due to
the decrease in melatonin.

When we think of the disease osteoporosis, we often attribute it to getting old.
Osteoporosis, however, is much more complex. Physiologically, the body undergoes a lot of
changes through the process of aging that relate to it, but it is these processes that
allow the world of medicine to find means to prevent and even sometimes treat
osteoporosis.

Osteoporosis is a condition of aging in which the density of bones in the body begins
to decrease. Although many people view bones as rather inactive tissues, they actually are
constantly in a flux known as turnover. This is the process by which the bone is
continually remodeled to produce new bone (Snow-Harter, 1993). Constant muscular and
weight bearing strain on the surface of the bone causes tiny stresses. These stresses get
attacked by osteoclasts, which bore into the stress on the surface of the bone. This
begins the process of resorption, during which the small hole almost triples in size. The
next phase is the beginning of reformation of the bone matrix. This occurs when
osteoblasts migrate to the cavity caused by resorption. The osteoblasts are responsible
for producing the matrix that composes the structure of the bone. Osteoblastic activity
also triggers calcium formation, which completes the formation of the bone. If this
continual process occurs under the right conditions, the bone can actually increase in
mass and density (Snow-Hartet, 1993). If conditions are not right, osteoporosis is the end
result. Improper conditions, which will be discussed later, lead to an imbalance of
osteoclastic and osteoblastic activity. If the resorption of bone is greater than the
reformation of the bone matrix, bone density decreases leading to the increased
susceptibility to fractures and other bone related injuries. (Snow-Hartet, 1993)

Better knowledge of the causes of osteoporosis leads to better treatment and
prevention. The medicinal treatments will be discussed but prevention is by far the most
cost effective (Wood, 1992). The easiest method of osteoporosis prevention is by a
continual and progressive regiment of weight bearing exercise. Among pre-menopausal women,
exercise is a fantastic way to promote bone and overall health of the body. As was
discussed before, the continual stress on the bone surface can lead to increased
osteoblastic reformation of the bone matrix. Exercise can also help women who have gone
through menopause. A study of 22 healthy post-menopausal women showed that those receiving
estrogen therapy actually increased bone density and mass after 22 months of exercise.
Lumbar spine bone density actually increased by 6.1 %. Women that were not put on a
workout plan showed a loss of bone (Wood, 1992).

Calcium consumption above the RDA value of 800 mg for adults is recommended to prevent
the onset of osteoporosis. This is increasingly important for elderly, post-menopausalwomen because they have a less efficient calcium uptake mechanism due to
aging. More supplemental calcium is required to improve absorption of the mineral (Wood,
1992). Calcium can also be used for treatment after the onset of osteoporosis. It was
observed that post-menopausal osteoporosis patients who received 1000 mg of supplemental
calcium a day showed a 50% decrease in non-vertebral bone loss (Wood, 1992). Some evidence
suggests that calcium supplementation can only benefit a female post-menopausal
osteoporosis patient if she is already undergoing estrogen therapy because estrogen helps
control the absorption of calcium. This argument continues but it is known that estrogen
therapy for osteoporosis patients is an effective treatment for the crippling disease.

There is powerful evidence that estrogen replacement maintains bone mass and reduces
the fracture risk of post-menopausal women (Snow-Harter, 1993). Supplemental estrogen
during the early years of menopause is effective in decreasing osteoporosis-related
injuries by upwards of 50% (Wood, 1992). This treatment also has been noted to work well
for women who have well-established osteoporosis. Results show that it can increase bone
mass by 3% by decreasing resorption and shifting the balance to the side of the more
favorable reformation (Wood, 1992).

Another anti-resorptive hormone that aids in decreasing the adverse effects of
osteoporosis is calcitonin. No evidence currently exists stating why the drug works well,
but trials do suggest that it is an effective agent in ceasing bone loss in patients with
high bone turnover. Unfortunately, the evidence of this drugs effects is unclear
plus it is a very expensive form of therapy.

Other drugs known for their anti-resorptive properties are bisphosphonates. These drugs
bind to hydroxyapatite crystals in the bones and remain in the bone for many years (Wood,
1992). These drugs seem to be effective at inhibiting resorption. This is done when they
get released from the bone surface, bind to the osteoclasts, and interfere with resorption
of the bone. The downside of these drugs is that they cause irritation in the digestive
system.

Other methods of treatment actually support the formation of bone instead of protecting
them from degradation. Sodium fluoride has been shown to increase bone density in the
spine by 8 percent/year and by 4 percent/year in the femur (Wood, 1992). Unfortunately
there is no evidence proving that this increased density is the same as bone strength. The
increased bone growth can be abnormal in structure and lead to mass that is not strong.

Growth Factors such as insulin growth factors I and II are being related to the
increased success of osteoblasts. This increase in osteoblast efficiency leads to
increased rates of bone formation. Unfortunately, like most new drugs, these growth
factors have adverse side effects. One issue that is raised is the ability for the factor
to couple with a bone-seeking compound that will successfully deliver the treatment to the
site (Wood, 1992).

The nice thing about knowing how a disease attacks the body is being able to take steps
to prevent it, and there are a lot of ways to deter osteoporosis. Science has shown that
exercise is the cheapest and one of the most effective ways to prevent osteoporosis. If
this is coupled with proper diet, calcium supplementation, and estrogen therapy, the
characteristic loss of bone mass and density from osteoporosis can actually be reversed.
The same theories that make prevention possible are being proven to make treatment
possible. Supplements like estrogen and calcium are sometimes very effective in stopping
resorption, which leads to bone loss. Other drugs like sodium fluoride are able to promote
the formation of new bone matrix. However, many of the treatments are experimental and
unproven to be reliable in a broad range of cases. There is hope though, and science and
medicine is well on its way to developing treatments to ease the pain of over 1.5 million
Americans a year (Wood, 1992). On the other hand, even if foolproof treatments did exist,
the only way that they could be effective is if people were educated about the disease.
Education and self responsibility is the key to catching this disease before it attacks
and for fighting it off if it does.